Evidence map›Paper›PMID 40936038›Full record

ArticleMolecular biotechnology2026

Data-Driven Discovery of a Key Regulator Cyclin A2 as a Promising Therapeutic Target in Hormone-Sensitive Cancers.

Suvitha Anbarasu, Anand Anbarasu

Abstract read
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In one paragraph

Article in Molecular biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Suvitha AnbarasuMedical and Biological Computing Laboratory, Department of Biotechnology, School of Biosciences and Technology (SBST), Vellore Institute of Technology (VIT), Vellore, 632014, Tamil Nadu, India.ORCID http://orcid.org/0000-0001-5204-6121
Anand AnbarasuMedical and Biological Computing Laboratory, Department of Biotechnology, School of Biosciences and Technology (SBST), Vellore Institute of Technology (VIT), Vellore, 632014, Tamil Nadu, India. aanand@vit.ac.in.ORCID http://orcid.org/0000-0003-2216-7488

Funding

Indian Council of Medical Research IRIS ID: 2021 10630
6 · The paper itself

Abstract

Hormone-sensitive cancers (HSCs) are one of the predominant types of cancer leading to death globally. The current study has attempted to discover a potential therapeutic target that could be used against HSCs in women, namely, breast, ovarian, and endometrial cancer. The differentially expressed genes in each cancer type were compared with previously reported tamoxifen resistance-causing genes. The hub genes CCNA2, CDCA8, ISG15, and E2F1 were found in breast cancer, CCNA2, CDCA8, CXCR4, and LYN were found in ovarian cancer, and CCNA2 and POLE2 were found in endometrial cancer. The clusters with the hub genes were screened for functional importance and were found to be significant in cell cycle regulation pathways. The expression significance, correlation, mutational profile, survival potency, treatment response status, and clinical profile revealed that CCNA2 was significantly associated with all three cancers. This study revealed that CCNA2 was positively correlated with other resistance-causing genes such as CENPE, MK167, CDCA8, NEK2, PRC1, ZWINT, CDKN3, MYBL2, and E2F1, in various cancers, validating its potential to cause resistance. Compared with other hub genes, CCNA2 had a Lower mutation percentage and critical hazard ratios of 2.16, 1.75, and 1.68 in breast, ovarian, and endometrial cancers, respectively, indicating its pivotal role in survival. The median CCNA2 expression level was 21.301 in stage IV BC patients, 38.481 in stage II ovarian cancer patients, and 23.206 in stage IV endometrial cancer patients. Thus, CCNA2 could be a potential therapeutic target for treating HSCs with endocrine therapy resistance.

Indexed as

Breast NeoplasmsCyclin A2Endometrial NeoplasmsOvarian NeoplasmsDrug Resistance, NeoplasmFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMutationCCNA2 protein, humanCyclin A2Cell cycleDifferential regulationDrug resistanceHormone dependentTarget screening

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.